B6;129-Kidins220tm1.2Fces/Cnrm
| Status | Available to order |
| EMMA ID | EM:14667 |
| International strain name | B6;129-Kidins220tm1.2Fces/Cnrm |
| Alternative name | Kidins220KO |
| Strain type | Targeted Mutant Strains : Knock-out |
| Allele/Transgene symbol | Kidins220tm1.2Fces, |
| Gene/Transgene symbol | Kidins220 |
Information from provider
| Provider | Fabrizia Cesca |
| Provider affiliation | Department of Life Sciences, University of Trieste |
| Additional owner | Prof Giampietro Schiavo, Department of Neuromuscular Diseases, UCL Queen Square Institute of Neurology, London, UK. |
| Genetic information | A Kidins220 cDNA (encoding exon 16 and downstream exons) and polyA cassette flanked by two loxP sites was inserted in the unique NruI site within exon 16 of the mKidins220 gene. In Kidins220lox/lox mice, Kidins220 mRNA is transcribed under the control of its endogenous promoter, generating the full-length protein. Female lox/lox mice were crossed with males expressing cre recombinase under the ubiquitous phosphoglycerate kinase promoter, which is active from early stages of embryogenesis (Cesca et al, Cell Death Diff, 2012). Thus, this mouse line carries the constitutive deletion of the Kidins220 protein. |
| Phenotypic information | Homozygous:When in homozygosis, embryos die at late stages of development, showing extensive cell death in the central and peripheral nervous system, as well as anomalies in the cardiovascular system (Cesca et al, Cell Death Diff 2012; Cesca et al, Cell Death Dis 2011).Heterozygous:The mouse strain kept in heterozygosis is viable, with normal life span and normal breeding capabilities. |
| Breeding history | Mice have been always bred on C57BL/6 background. |
| References |
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| Homozygous fertile | no |
| Homozygous viable | no |
| Homozygous matings required | no |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | CNR, Consiglio Nazionale delle Ricerche, Monterotondo, Italy |
Disease and phenotype information
Orphanet associated rare diseases, based on orthologous gene matching
- Spastic paraplegia-intellectual disability-nystagmus-obesity syndrome / Orphanet_521390
Literature references
- Kidins220/ARMS is an essential modulator of cardiovascular and nervous system development.;Cesca F, Yabe A, Spencer-Dene B, Arrigoni A, Al-Qatari M, Henderson D, Phillips H, Koltzenburg M, Benfenati F, Schiavo G, ;2011;Cell death & disease;2;e226; 22048169
- Kidins220/ARMS mediates the integration of the neurotrophin and VEGF pathways in the vascular and nervous systems.;Cesca F, Yabe A, Spencer-Dene B, Scholz-Starke J, Medrihan L, Maden C H, Gerhardt H, Orriss I R, Baldelli P, Al-Qatari M, Koltzenburg M, Adams R H, Benfenati F, Schiavo G, ;2012;Cell death and differentiation;19;194-208; 22048155
- A developmental stage- and Kidins220-dependent switch in astrocyte responsiveness to brain-derived neurotrophic factor.;Jaudon Fanny, Albini Martina, Ferroni Stefano, Benfenati Fabio, Cesca Fabrizia, ;2021;Journal of cell science;134;18045-18055; 34279618
- Functional Interaction between the Scaffold Protein Kidins220/ARMS and Neuronal Voltage-Gated Na+ Channels.;Cesca Fabrizia, Satapathy Annyesha, Ferrea Enrico, Nieus Thierry, Benfenati Fabio, Scholz-Starke Joachim, ;2015;The Journal of biological chemistry;290;e35785; 26037926
- Kidins220/ARMS is a novel modulator of short-term synaptic plasticity in hippocampal GABAergic neurons.;Scholz-Starke Joachim, Cesca Fabrizia, Schiavo Giampietro, Benfenati Fabio, Baldelli Pietro, ;2012;PloS one;7;1505-1519; 22563401
- Kidins220/ARMS controls astrocyte calcium signaling and neuron-astrocyte communication.;Jaudon Fanny, Chiacchiaretta Martina, Albini Martina, Ferroni Stefano, Benfenati Fabio, Cesca Fabrizia, ;2020;Cell death and differentiation;27;; 31624352